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Mitochondrial Therapy for Parkinson Disease

Mitochondrial Therapy for Parkinson Disease EDITORIAL HE PRECISE causes of Parkinson disease however, the greatest effect was in the highest dosage of (PD) are beginning to be defined and in- 1200 mg/d. clude specific genetic mutations causal of Their data are supportive of the view that mitochon- autosomal dominant (alpha-synuclein mu- drial dysfunction does play a role in the pathogenesis of T tations) and recessive (Parkin muta- sporadic PD and that further research using coenzyme tions) phenotypes and for sporadic PD, an interaction be- Q at higher dosages should be studied. It will be im- 1,2 tween genetic and environmental factors. An important portant to define whether the defects of mitochondrial emerging molecular defect is impaired function of the mi- complexes I and II/III are acquired genetic mutations and tochondrial electron transport chain, particularly inhi- whether they are due to environmental toxins or pri- bition of complexes I and II/III, leading to failure of aden- mary congenital mutations, inherited maternally, which osine triphosphate synthesis. Inhibition of complex I by cause a genetic predisposition for PD. Clearly, the data MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) of the Parkinson Study Group in this article are intrigu- 3,4 can cause human parkinsonism. Schapira and col- ing and provocative therapeutic findings and http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Neurology American Medical Association

Mitochondrial Therapy for Parkinson Disease

JAMA Neurology , Volume 59 (10) – Oct 1, 2002

Mitochondrial Therapy for Parkinson Disease

Abstract

EDITORIAL HE PRECISE causes of Parkinson disease however, the greatest effect was in the highest dosage of (PD) are beginning to be defined and in- 1200 mg/d. clude specific genetic mutations causal of Their data are supportive of the view that mitochon- autosomal dominant (alpha-synuclein mu- drial dysfunction does play a role in the pathogenesis of T tations) and recessive (Parkin muta- sporadic PD and that further research using coenzyme tions) phenotypes and for sporadic PD, an...
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Publisher
American Medical Association
Copyright
Copyright 2002 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.
ISSN
2168-6149
eISSN
2168-6157
DOI
10.1001/archneur.59.10.1523
Publisher site
See Article on Publisher Site

Abstract

EDITORIAL HE PRECISE causes of Parkinson disease however, the greatest effect was in the highest dosage of (PD) are beginning to be defined and in- 1200 mg/d. clude specific genetic mutations causal of Their data are supportive of the view that mitochon- autosomal dominant (alpha-synuclein mu- drial dysfunction does play a role in the pathogenesis of T tations) and recessive (Parkin muta- sporadic PD and that further research using coenzyme tions) phenotypes and for sporadic PD, an interaction be- Q at higher dosages should be studied. It will be im- 1,2 tween genetic and environmental factors. An important portant to define whether the defects of mitochondrial emerging molecular defect is impaired function of the mi- complexes I and II/III are acquired genetic mutations and tochondrial electron transport chain, particularly inhi- whether they are due to environmental toxins or pri- bition of complexes I and II/III, leading to failure of aden- mary congenital mutations, inherited maternally, which osine triphosphate synthesis. Inhibition of complex I by cause a genetic predisposition for PD. Clearly, the data MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) of the Parkinson Study Group in this article are intrigu- 3,4 can cause human parkinsonism. Schapira and col- ing and provocative therapeutic findings and

Journal

JAMA NeurologyAmerican Medical Association

Published: Oct 1, 2002

References

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